重组RA538、反义c-myc腺病毒对不同细胞系转染效率与作用及其机制的研究

腺病毒载体研究的发展使基因治疗付诸于临床应用成为可能,它以遗传毒性低、致病性小、宿主范围广、滴度高、装载容量大等优势已广泛用于基因治疗。腺病毒载体能感染增生分裂细胞及非增生分裂细胞,相同的腺病毒载体对不同的靶细胞可能会产生不同的作用,阐明腺病毒载体转染效率及疗效之间存在的关系及其机制具有重要意义。我们的研究发现腺病毒（ａｄｅｎｏｖｉｒｕｓ,Ａｄ）介导的ＲＡ５３８、反义（ａｎｔｉｓｅｎｓｅ,ＡＳ）ｃ－ｍｙｃ具有抑制人胃癌细胞生长、诱导其凋亡及下调节ｃ－ｍｙｃ、ｂｃｌ－２基因表达的作用（另文发表）。…     

重组腺病毒介导反义c-myc基因对人肝癌细胞系的治疗作用

目的：探讨重组腺病毒介导反义ｃ－ｍｙｃ基因（Ａｄ－ＡＳｍｙｃ）治疗人肝癌细胞的作用。方法：观察Ａｄ－ＡＳｍｙｃ对人肝癌细胞系的转导效率,通过细胞生长曲线、克隆形成实验、ＤＮＡ片段化分析、ＲＴ－ＰＣＲ、裸鼠皮下移植瘤治疗实验,分析Ａｄ－ＡＳｍｙｃ对人肝癌细胞系Ｂｅｌ－７４０２、ＱＳＧ－７７０１、ＳＭＭＣ－７７２１和ＨＣＣ－９２０４细胞生长和ｃ－ｍｙｃ基因表达及裸鼠肿瘤生长的抑制作用。结果：Ａｄ－ＡＳｍｙｃ可高效转导人肝癌细胞系,抑制细胞生长;转染细胞克隆形成能力降低,克隆成活率为对照组的５３．９％～６９．１％,ｃ－ｍｙｃ基因表达下降;Ａｄ－ＡＳｍｙｃ处理肝癌细胞,ＤＮＡ凝胶电泳出现明显的梯形条带,瘤内注射Ａｄ－ＡＳｍｙｃ可抑制裸鼠皮下移植瘤生长。结论：重组腺病毒介导的反义ｃ－ｍｙｃ基因转移,有可能成为肝癌基因治疗     

反义转染细胞HL^R60—9的c—myc基因表达及其生物大分子的…

作者构建了体外能双向转录ｃ－ｍｙｃ基因的重组质粒ＰＧＣ，以制备ＲＮＡ探针用于检测ｃ－ｍｙｃ反义ＲＮＡ转染细胞ＨＬ＾Ｒ６０－９的ｃ－ｍｙｃ及反义ＲＮＡ表达，结果显示，Ｃｄ＾２＋诱导的ＨＬ＾Ｒ６０－９细胞的ｃ－ｍｙｃ反义ＲＮＡ表达随Ｃｄ＾２＋浓度及作用时间的增加而增强，但ｃ－ｍｙｃｍＲＮＡ表达在诱导过程中逐渐减少，两者变化呈镜相关系。免疫组化法未能检出ｃ－ｍｙｃＰ６２蛋白的表达，＾３Ｈ－ＴｄＲ，＾３Ｈ     

反义bcl-2基因转染对单核白血病细胞存活及化疗耐受能力的影响

目的：探讨ｂｃｌ－２反义核酸在单核白血病细胞系Ｕ９３７细胞中的作用,以丰富ｂｃｌ－２及其反义核酸调控肿瘤细胞凋亡的资料。方法：将反义ｂｃｌ－２基因表达载体ｐＬＸＳＮ／ａｓ－ｂｃｌ－２转染于Ｕ９３７细胞,建立Ｕ９３７／ａｓ－ｂｃｌ－２细胞模型,利用流式细胞技术模型细胞ｂｃｌ－２的表达水平。通过细胞计数观察模型细胞在正常培养条件下和有化疗药物Ａｒａ－Ｃ或三     

bcl—2反义寡核苷酸抑制HL—60细胞增殖的研究

目的 研究ｂｃｌ－２反义寡核苷酸在抑制ＨＬ－６０细胞增殖和下调细胞内ｂｃｌ－２蛋白表达水平的作用。方法 将人工合成的ｂｃｌ－２反义寡核苷酸片段与ＨＬ－６０细胞共培养,在作用的第０天,１天,３天,５天通过细胞计数和锥虫蓝染色法检测细胞的生长,存活情况,同时通过免疫组化法（ＡＰＡＡＰ法）检测细胞内ｂｃｌ－２蛋白表达水平的变化情况,结果 ｂｃｌ－２正,反义寡核革酸均可抑制ＨＬ－７０细胞增但ｂｃｌ－２反义     

高表达bcl-2卵巢癌细胞系参与药物抵抗和细胞凋亡作用的研究 *

目的：探讨化疗的敏感性与细胞凋亡的关系,观察细胞凋亡抑制分子ｂｃｌ－２在卵巢癌化疗抵抗中的作用。方法：构建了逆转录病毒ｂｃｌ－２表达载体ｐＬＸＳＮ／ｂｃｌ－２,应用ｌｉｐｏｆａｃｔｉｎ法建立转染ｂｃｌ－２基因和转染空载体ｐＬＸＳＮ的卵巢癌细胞系。ＭＴＴ法观察细胞系抵抗药物的细胞毒作用。ＦＡＣＳ和ＤＮＡ琼脂糖凝胶电泳观察ｂｃｌ－２高表达细胞系在阿霉素诱导细胞凋亡中的变化。结果：转染 ｂｃｌ－２的卵巢癌细胞系ＯＣ３／ｂｃｌ－２稳定表达ｂｃｌ－２分子并抵抗药物介导的细胞毒作用,明显提高细胞的存活率,与此同时也抑制细胞凋亡的发生。结论：化疗的敏感性与细胞凋亡的调节密切相关,凋亡抑制基因ｂｃｌ－２在肿瘤耐药中起重要作用。     

反义转染细胞HL_（60）~R－9的c-myc基因表达及其生物大分子的生物合成

作者构建了体外能双向转录ｃ－ｍｙｃ基因的重组质粒ＰＧＣ，以制备ＲＮＡ探针用于检测ｃ－ｍｙｃ反义ＲＮＡ转染细胞ＨＬＲ６０－９的ｃ－ｍｙｃｍＲＮＡ及反义ＲＮＡ表达。结果显示，Ｃｄ２＋诱导的ＨＬＲ６０－９细胞的ｃ－ｍｙｃ反义ＲＮＡ表达随Ｃｄ２＋浓度及作用时间的增加而增强，但ｃ－ｍｙｃｍＲＮＡ表达在诱导过程中逐渐减少，两者变化呈镜相关系。免疫组化法未能检出ｃ－ｍｙｃＰ６２蛋白的表达。３Ｈ－ＴｄＲ、３Ｈ－ＵＲ及３Ｈ－Ｌｅｕ掺入试验表明其ＤＮＡ、ＲＮＡ及蛋白质生物合成明显抑制。以上结果表明，ＨＬＲ６０－９细胞的恶性表型逆转及现所示的大分子生物合成抑制，与ｃ－ｍｙｃ反义ＲＮＡ阻断了ｃ－ｍｙｃｍＲＮＡ表达有关。     

泰素帝诱导人肺腺癌细胞凋亡的实验研究

目的 探讨泰素帝诱导人肺腺癌细胞凋亡的作用机制。方法 应用形态学方法、流式细胞术（ＦＡＣＳ）、ＤＮＡ凝胶电泳、ＡｎｎｅｘｉｎＶ标记等方法检测细胞凋亡的发生,应用ＲＴ－ＰＣＲ检测凋亡相关基因Ｆａｓ、ｂｃｌ－２、ｃ－ｍｙｃ表达的变化。结果 泰素帝对人肺腺癌细胞系Ａ５４９细胞的生长有明显的抑制作用,使细胞分裂阻滞于Ｇ２Ｍ期,并诱导肿瘤细胞发生凋亡。凋亡细胞表现为细胞固缩,核染色质聚集或断裂,ＤＮＡ凝胶电     

腺病毒介导的RA538基因转移及其对人结肠癌细胞

目的 进上步研究ＲＡ５３８对人结肠癌细胞生物学效应，选用介导ＲＡ５３８重组体腺病毒，观察其对人结肠癌细胞系ＨＣＴ的作用。方法 通过重组体腺病毒将ＰＡ５３８基因转导到人结肠癌细胞系ＨＣＴ中，观察转染ＲＡ５３８基因后的肿瘤细胞生长情况。经流式细胞仪、ＤＮＡ片段化分析及ＴＵＮＥＬ检测分析抑瘤机制。结果 由重组体腺病毒Ａｄ－ＲＡ５３８介导基因ＲＡ５３８转导在ＨＣＴ获得较主的转导效率，ＭＯＩ为１００时使８０     

凋亡相关基因bcl—x,bax在霍奇金病中的表达及其意义

目的 探讨凋亡相关基因ｂｃｌ－ｘ，ｂａｘ在霍奇金病Ｒ－Ｓ细胞凋亡调控中的作用及其意义，方法 采用免疫组化法检测ｂｃｌ－ｘ，ｂａｘ基因在霍金奇病组织中的表达；应用免疫荧光双标记，激光共聚焦显微镜下检测ｂｃｌ－２，与上述基因是否在同一Ｒ－Ｓ细胞内共表达，结果：８５．４％，７０．８％的霍奇金病例Ｒ－Ｓ细胞及霍奇金医院ｂｃｌ－ｘ，ｂａｘ阳性，ｂｃｌ－２与ｂｃｌ－ｘ，ｂｃｌ－２和ｂａｘ可以共存同一Ｒ－Ｓ细胞     

腺病毒介导的RA538基因转移及其对人结肠癌细胞HCT的抑瘤作用

目的　进一步研究ＲＡ５３８ 对人结肠癌细胞系的生物学效应,选用介导ＲＡ５３８ 重组体腺病毒,观察其对人结肠癌细胞系ＨＣＴ 的作用。方法　通过重组体腺病毒将ＲＡ５３８ 基因转导到人结肠癌细胞系ＨＣＴ 中,观察转染ＲＡ５３８ 基因后的肿瘤细胞生长情况。经流式细胞仪、ＤＮＡ 片段化分析及ＴＵＮＥＬ 检测分析抑瘤机制。结果　由重组体腺病毒ＡｄＲＡ５３８ 介导基因ＲＡ５３８ 转导在ＨＣＴ 获得较高的转导效率, ＭＯＩ 为１００ 时可使８０ ％ 细胞转染,并显示对肿瘤细胞生长有明显的抑制作用,抑制率为７４ ％ 。裸鼠皮下注射ＲＡ５３８ 处理的ＨＣＴ 细胞肿瘤形成能力为２０ ％ 。ＤＮＡ 片段化分析、ＴＵＮＥＬ 和流式细胞仪检测,结果证明ＲＡ５３８诱导肿瘤细胞发生凋亡。Ｗｅｓｔｅｒｎ ｂｌｏｔ 分析表明,ＲＡ５３８ 具有明显下调ｃｍ ｙｃ 基因表达的作用。结论　ＲＡ５３８ 对人结肠肿瘤细胞有抑制生长和诱导凋亡的作用,可以作为结肠肿瘤基因治疗的１ 种新的治疗基因。     

腺病毒介导RA538基因转移及其对肿瘤的抑制作用

目的:RA538是从维甲酸诱导终末分化的人食管癌细胞系中分离出的一个与分化相关的基因,本研究探讨了其抗癌作用.方法:利用腺病毒介导基因转移观察对肿瘤细胞的抑制效应.结果:通过重组体腺病毒将RA538基因转导到人肺腺癌细胞系(GLC-82)和人结肠癌细胞系(HCY)中,获得较高的转导效率,显示出较明显的抑制肿瘤生长作用,抑制率分别为77.2%和77.9%,并能降低两细胞系体内肿瘤形成能力.流式细胞计数、DNA片段化分析及TUNEL检测证实RA538可诱导肿瘤细胞发生凋亡.Westem blot分析表明,RA538具有明显下调c-myc基因表达的作用,结论:研究结果提示,RA538是一个较广谱的抑癌基因,可以作为肿瘤基因治疗的一个新目的基因,具有良好的应用前景.     

携带反义c-myc的重组腺病毒安全性研究

目的　研究携带反义c myc的重组腺病毒 (Ad ASmyc)潜在的副作用 ,评价其安全性 ,为其进一步进入临床试验提供依据。方法　用Ad ASmyc感染HeLa细胞 ,制备细胞提取液后反复两次感染HeLa细胞 ,观察Ad ASmyc的繁殖、扩增 ,以及对HeLa细胞的作用 ,RT PCR检测其DNA的转录 ;确定Ad ASmyc对作为正常细胞的人胚肺二倍体细胞 2BS的感染能力 ,绘制细胞生长曲线 ,观察Ad ASmyc对正常细胞的毒性 ;给Balb/c小鼠腹腔注射重组腺病毒后 ,每日观察一般状况 ,化验肝、肾功能 ,PCR检测Ad ASmyc在重要脏器中的分布 ,显微镜观察重要脏器的病理学变化。结果　Ad ASmyc是一复制缺陷型腺病毒 ,它能高效感染 2BS细胞 ,但并不影响其生长 ,小鼠体内应用后 ,无急性毒性症状发生 ,在肝、肾、胃、脾内可检测到腺病毒的分布。但在注射 10 9pfu第 6天、第 12天的小鼠肝组织内可观察到轻微炎症。结论　Ad ASmyc应用是安全的 ,可以进入临床试验。     

pRb-expressing adenovirus Ad5-Rb attenuates the p53-induced apoptosis in cervical cancer cell lines

The retinoblastoma protein (pRb), the gene product of the first reported tumour suppressor gene, is functionally inactivated by the E7 protein of high-risk human papillomavirus (HPV) found in most human cervical cancers. We have, in this study, constructed an adenoviral vector expressing wild-type pRb (Ad5-Rb) and used the constructed Ad5-Rb to transfect the osteosarcoma cell line Saos-2, and three cervical cancer cell lines HeLa, SiHa and C-33A. Our results showed that pRb caused G1 arrest in Saos-2 cells after transfection with Ad5-Rb. The number of colonies formed by the Ad5-Rb-transfected Saos-2 cells in soft agar was also found to be significantly lower (P<0.05) than those transfected with the adenoviral control expressing Escherichia coli β-galactosidase (Ad5-LacZ). The transfection of Ad5-Rb caused an increase in the population of SiHa and C-33A cells in the G1 phase from 53.0 and 52.9% to 72.4 and 64.3%, respectively, but not in the HeLa cells. However, Ad5-Rb did not show any inhibitory effect on the growth of SiHa, HeLa and C-33A cells, and inhibition of colony formation in soft agar was not observed either. In contrast, flow cytometric analysis showed that Ad5-p53, a p53-expressing adenovirus, induced apoptosis, i.e. the appearance of sub-G1 peak, in all three tested cervical cancer cell lines. Nevertheless, the Ad5-p53-induced apoptosis was partially inhibited when Ad5-Rb was added simultaneously. These findings suggested that pRb may not be a good candidate for cervical cancer gene therapy. Our data also showed that the use of full-length pRb in combination with TP53 might not be a suitable strategy for cancer gene therapy.     

bcl-2反义寡核苷酸对肾癌细胞Bcl-2蛋白表达抑制及诱导凋亡作用

目的:经Beagle犬肝脏血管注射重组腺病毒介导反义c-myc基因(Ad-ASmyc)载体,观测其体内分布及毒副作用,以评价Ad-ASmyc治疗肝癌的临床前期安全性.方法:选择4只体重8～10kg健康Beagle犬,全麻后开腹,经肝动脉或门静脉注射Ad-ASmyc,注射Ad-ASmyc前及注射后第3,7,14,21天取肝组织及抽取静脉血化验,PCR检测Ad-ASmyc在各器官组织中的分布,常规切片观察各器官病理变化,ELISA方法检测血中抗腺病毒抗体的产生.结果:经Beagle犬肝脏血管注射后,Ad-ASmyc可持续转导正常肝细胞达3周,实验犬一般情况好,血、肝、肾功能无明显异常,在肝脏、脾脏、肾脏、胃、心脏、皮肤中可检测到重组腺病毒的分布,镜下可见Ad-ASmyc剂量依赖性的肝组织轻微的炎症反应,注射后7d血中有抗腺病毒载体的抗体产生,14d达高峰,21d开始下降.结论:经Beagle犬肝动脉或门静脉途径注射Ad-ASmyc均可转导至肝细胞,Ad-ASmyc对实验犬的毒副作用较轻.     

三氧化二砷诱导胃癌细胞凋亡及对相关基因表达的影响

目的 研究三氧化二砷（As2O3)诱导胃癌细胞的凋亡作用及对凋亡相关基因p53、c-myc、bcl-2、bcl-xl和bcl-xs表达的影响,探讨其诱导胃 癌凋亡的作用机制。方法 研究As2O3对胃癌细胞SGC－07901和MKN－45的诱导凋亡作用和对凋亡相关基因表达的影响。结果 As2O3作用于细胞可见典型的细胞凋亡。出现典型的亚二倍体“凋亡峰”。10μmol／LAs2O3的诱导胃癌细胞SGC－7901和MKN－45的凋亡率为13．8％和22．5％。细胞凋亡指数在1．42％－9．5％之间。As2O3作用后能明显下调SGC－7901细胞的bcl-2蛋白和mRNA的表达;对SGC－7901细胞的p53、c-myc、bcl-xl和bcl-xs蛋白的表达无影响。As2O3能促进MKN－45细胞的p53蛋白和mRNA的表达,对MKN－45细胞的bcl-2、c-myc、bcl-xl和bcl-xs基因表达无影响。结论 As2O3可通过不同途径诱导胃癌细胞凋亡,通过下调SGC－7901细胞的bcl-2的蛋白表达诱导其凋亡,通过上调p53表达诱导胃癌MKN－45细胞凋亡。     

RGD修饰的腺病毒介导LIF和IL-24双基因共表达对MEG01白血病细胞的抑制作用

目的 利用RGD修饰改造白血病抑制因子（LIF）和白细胞介素 24（IL-24）双基因共表达腺病毒载体,以提高感染效率,探讨其对人白血病MEG01细胞的抑制作用。方法 同源重组法构建RGD修饰的表达LIF、IL 24的腺病毒载体Ad.RGD-LIF、Ad.RGD -IL24和Ad.RGD-LIF-IL24。在QBI-293A细胞中扩增腺病毒,检测病毒滴度。流式细胞仪检测各组腺病毒载体对MEG01细胞的感染效率。应用Western blotting检测目的基因LIF、IL-24在MEG01细胞中的表达。CCK-8法检测各组腺病毒载体Ad.RGD-LIF、Ad.RGD-IL24、Ad.RGD-LIF-IL24感染MEG01细胞后对细胞增殖的影响。PE-AnexinV／7-AAD双染后,经流式细胞仪检测细胞凋亡的变化。Western blotting检测凋亡相关蛋白的表达。PI染色后,流式细胞仪检测目的基因表达对MEG01细胞周期的影响。实时定量PCR检测细胞周期调控基因p21和E2F1的表达。结果 成功构建了RGD修饰的腺病毒载体Ad.RGD-LIF、Ad.RGD-IL24和Ad.RGD-LIF-IL24。RGD修饰后的腺病毒能够显著增强对MEG01细胞的感染效率。CCK-8检测显示,与PBS组比较,携带单个目的基因的腺病毒载体Ad.RGD-LIF和Ad.RGD-IL24在第5 d对细胞生长的抑制率分别为29.2％和31.5％,均能够显著抑制MEG01细胞的生长;携带Ad.RGD-LIF-IL24双基因组的抑制率达42.5％,优于单基因组,差异均有统计学意义（P＜0.05）。凋亡检测显示,与PBS组（4.5％）和空病毒组Ad.RGD（7.4％）比较,Ad.RGD-IL24（20.9％）、Ad.RGD LIF（17.8％）均能够显著促进细胞凋亡,且Ad.RGD-LIF-IL24双基因组（29.7％）的促凋亡作用更强。Western blotting显示,LIF和IL-24能够提高促凋亡蛋白p53、Bax的表达,同时抑制抗凋亡蛋白Bcl-xl的表达。目的基因LIF、IL-24过表达会影响MEG01细胞周期的进程,使细胞阻滞在G2期。实时定量PCR显示,LIF和IL-24能够上调细胞周期调控基因p21的转录,抑制E2F1的表达。结论LIF和IL-24过表达的腺病毒载体在体外通过调节p53、Bax、Bcl-xl的表达,影响白血病细胞MEG01的生长,诱导其凋亡,并通过调控p21、E2F1的水平影响细胞周期的进程。     

Differential suppression of human cervical cancer cell growth by adenovirus delivery of p53 in vitro: arrest phase of cell cycle is dependent on cell line.

It has been reported that overexpression of wild-type p53 protein induces suppression of tumor cell growth in vivo and in vitro. In this study, we further evaluated the differential effects of p53 delivered in an adenovirus vector on the cell growth, apoptosis and cell cycle progression in cervical cancer cell lines. We constructed a recombinant adenovirus expressing p53 and then delivered this into cervical carcinoma cell lines (CaSki, SiHa, and HeLa, HeLaS3) along with adenovirus expressing beta-galactosidase as a negative control. Adenovirus-delivered p53 overexpression resulted in a more significant suppression of cell growth in HPV 18-infected cells (HeLa and HeLaS3) and a lesser suppression in HPV 16-infected cells (CaSki and SiHa). However, no suppression was observed in cells infected with a negative control virus. p53 overexpression also induced apoptosis and cell cycle arrest, as determined by annexin V and propidium iodide staining. In particular, the cell cycle was arrested in the G(2)/M phase in CaSki cells. In contrast, cell cycles were arrested in the G(1) phase in HeLa cells, suggesting that the arrest phase is dependent upon the cervical cancer cell line. Taken together, these data support the idea that overexpressed p53 protein plays a differential role in suppressing cervical cancer cell growth through apoptosis and cell cycle arrest in either G(1) or G(2)/M phase, depending on the cancer cell line.     

Differential Suppression of Human Cervical Cancer Cell Growth by Adenovirus Delivery of p53 in vitro: Arrest Phase of Cell Cycle Is Dependent on Cell Line

It has been reported that overexpression of wild-type p53 protein induces suppression of tumor cell growth in vivo and in vitro. In this study, we further evaluated the differential effects of p53 delivered in an adenovirus vector on the cell growth, apoptosis and cell cycle progression in cervical cancer cell lines. We constructed a recombinant adenovirus expressing p53 and then delivered this into cervical carcinoma cell lines (CaSki, SiHa, and HeLa, HeLaS3) along with adenovirus expressing β-galactosidase as a negative control. Adenovirus-delivered p53 overexpression resulted in a more significant suppression of cell growth in HPV 18-infected cells (HeLa and HeLaS3) and a lesser suppression in HPV 16-infected cells (CaSki and SiHa). However, no suppression was observed in cells infected with a negative control virus. p53 overexpression also induced apoptosis and cell cycle arrest, as determined by annexin V and propidium iodide staining. In particular, the cell cycle was arrested in the G₂/M phase in CaSki cells. In contrast, cell cycles were arrested in the G₁ phase in HeLa cells, suggesting that the arrest phase is dependent upon the cervical cancer cell line. Taken together, these data support the idea that overexpressed p53 protein plays a differential role in suppressing cervical cancer cell growth through apoptosis and cell cycle arrest in either G₁ or G₂/M phase, depending on the cancer cell line.     

Selective effects of a fiber chimeric conditionally replicative adenovirus armed with hep27 gene on renal cancer cell

Adenoviruses mediated cancer gene therapies are widely investigated and show a promising effect on cancer treatment. However, efficient gene transfer varies among different cancer cell lines based on the expression of coxsakie adenovirus receptor (CAR). Hep27, a member of dehydrogenase/reductase (SDR) family, can bind to Mdm2, resulting in the attenuation of Mdm2-mediated p53 degradation. Here we constructed a fiber chimeric adenovirus carrying hep27 gene (F5/35-ZD55-Hep27), in which the fiber protein of 5-serotype adenovirus (Ad5) was substituted by that of 35-serotype adenovirus (Ad35), aiming to facilitate the infection for renal cancer cells and develop the role of hep27 in cancer therapy. We evaluated the CAR and CD46 (a membrane cofactor protein for Ad35) expression in four kinds of renal cancer cells and assessed the relationship between receptors and infection efficiency. 5/35 fiber-modified adenovirus had a much promising infectivity compared with Ad5-based vector in renal cancer cells. F5/35-ZD55-Hep27 had enhanced antitumor activity against human renal cancer cells compared to the other groups. Further, hep27 mediated p53 and cleaved-PARP upregulation and mdm2 downregulation was involved and caused increased apoptosis. Moreover, F5/35-ZD55-Hep27 significantly suppressed tumor growth in subcutaneous renal cancer cell xenograft models. Our data demonstrated that 5/35 fiber-modified adenovirus F5/35-ZD55-Hep27 transferred into renal cancers efficiently and increased p53 to induce cancer cell apoptosis. Thus 5/35 fiber-modified adenoviral vector F5/35-ZD55-Hep27 might a promising vector and antitumor reagent for renal cancer gene therapy.